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Diagnosis and Pathophysiology
The diagnosis is asthma. The main etiologic factor is a genetic predisposition to type 1 hypersensitivity. This results in acute inflammation which eventually leads to chronic inflammation of the airways and hyper responsiveness of the bronchial mucosa to various stimuli (Mims, 2015). Airway inflammation involves various inflammatory cells and inflammatory mediators, but type 2 T helper cells play a significant role in causing asthma. There is an excessive type 2 T helper cell reaction directed against various environmental antigens. These cells produce cytokines, especially interleukin-4 that stimulates the production of IgE, interleukin-5 that activates eosinophils, and interleukin-13 that stimulates the production of mucus and contributes to the stimulation of the production of IgE by B cells. Once these mast cells are exposed to specific allergens, they release the contents of their granules, leading to two types of reactions: early and late phase reactions.
An early reaction is characterized by vasodilation of various degrees, bronchoconstriction, and increased production of mucus. Bronchoconstriction results from stimulation of vagal receptors located below the epithelium by the monoamines released from mast cell granules. A late reaction is characterized by inflammation mediated by activated T cells, eosinophils, and neutrophils. Repeated episodes of inflammation lead to airway remodeling characterized by structural changes in the walls of the bronchi. These changes are increased vascularity, hypertrophy of bronchial mucus glands and smooth muscle, and deposition of collagen below the epithelium. These changes lead to increased resistance to the passage of air within the bronchial tree resulting in the characteristic features of asthma such as difficulty in breathing and wheezing.
Non-Pharmacologic and Pharmacologic Interventions
Non-Pharmacologic Interventions
The best non-pharmacologic intervention that will prevent asthma attacks and exacerbations is the avoidance of allergens. These could be certain foods, animal fur, pollen, or dust mites. Once the trigger is identified, modifications are made to the patients environment, especially the home, to reduce the concentration of the trigger (Milligan, Matsui, & Sharma, 2016). Modifications include removing items that trap dust such as rugs and upholstered furniture, cleaning floors with a damp cloth, regular changing and cleaning of bedding, and use of mite-resistant mattress covers.
Physical activity is essential for patients with asthma. It improves both lung and heart function. However, sometimes physical exertion may trigger asthmatic attacks. Therefore, the physician must work with the patient and her caregiver to select activities that are appropriate for her levels of fitness.
Pharmacological Interventions
Pharmacologic management of asthma is composed of short-term relief of symptoms and long-term control (Wang et al., 2017). The short-term relief is given using drugs that cause relaxation of bronchial smooth muscles and reduction of the secretions produced by the epithelium. Beta-adrenoceptor agonists are most effective for this. Others are anti muscarinic agents. Long-term control is attained using anti-inflammatory agents like inhaled corticosteroids.
Inhaled beta-adrenoceptor agonists such as albuterol act on beta 2 receptors on the respiratory smooth muscle causing relaxation. They also inhibit the release of inflammatory mediators from effector cells. The inhaled route is preferred because beta-adrenoceptor agonists have other systemic effects such as causing skeletal muscle tremors and tachycardia. This is because beta receptors are also present on cardiac muscle fibers and skeletal muscle. They have weak protein binding and low oral bioavailability. Also, they have a high renal clearance. Their short half-lives imply they can only be used for rapid, short-term relief of the symptoms.
Antimuscarinic agents competitively inhibit the action of acetylcholine at its receptors. Acetylcholine is released by vagal nerves causing increased secretion of mucus and smooth muscle contraction (Blake & Raissy, 2018). Antimuscarinic agents such as ipratropium bromide prevent this response and therefore cause bronchodilation and decreased secretions. Inhalation prevents the central nervous and gastrointestinal adverse effects of antimuscarinic agents. They have a longer half-life than beta-agonists hence they are given in combination or monotherapy when there is hypersensitivity to the agonists. It has a longer duration of action. Ipratropium is poorly absorbed across the pulmonary membranes, thus limiting its systemic effects.
Inhaled corticosteroids prevent the occurrence of the late phase inflammatory reaction by inhibiting chemotaxis. This is specifically through the inhibition of the release of leukotriene B4. The drugs are usually composed of small particles. They have a high affinity for the receptor and a long pulmonary residence time. These prolong its effects. They may be given as a prodrug which is activated by esterases in the pulmonary system. Activation in the lungs limits oral bioavailability and thus systemic effects. They are also rapidly cleared to prevent unwanted events. They should have a high plasma protein binding to prevent diffusion into other body tissues. Inhaled corticosteroids with hydroxyl moieties at the 21 position can bind to fatty acids present in the pulmonary system. These conjugates cannot be absorbed into the body thus potentiating their local action.
Resources Available in Tampa, Florida
The state of Florida has asthma-friendly child care centers. They are approved by the Florida Asthma Coalition. However, Hillsborough County does not have such a center. Instead, it has a mentor, Mary Martinasek from the University of Tampa, who may help child care centers to become certified by the Florida Asthma Coalition. She is also in charge of the Tampa Bay Asthma Coalition which provides outreach and community education. Shriners Hospital for Children and St Josephs Childrens Hospital are recognized asthma-friendly hospitals in Tampa by the Florida Asthma coalition.
Communication Plan
Involving children in their treatment and also effective communication with them has significant effects on their adherence to treatment (Klok, Kaptein, & Brand, 2015). In chronic conditions such as asthma, children need to take charge of taking their medication and thus must be guided appropriately.
Communication to the child involves a simplified description of the condition with the assurance that it is manageable. The child is encouraged to play an active role in their treatment. She will be taught to recognize triggers that cause exacerbations and how to avoid them. She will also be taught how to recognize an attack, what medication to take, and how to take it. Since in most cases an inhaler is given, the child will be taught to correctly activate and use an inhaler and also detect when the medication is almost finished to get a timely replacement. The child will also be educated on behavior modification such as increased hygienic vigilance and anticipation of attacks.
The mother will be encouraged to create a partnership with the patient. She will play a more supporting role while allowing the child to take charge of management. The mother will be responsible for the home and environment modification. She will be required to take the child along when collecting replacement medication so that the child can receive counseling from the community pharmacist. The mother will also be responsible for booking and keeping regular check-up appointments for the child. Finally, she will be the childs emergency contact and the first responder in case of attack; therefore, the training on selection and use of medication will involve both the mother and the child.
References
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Blake, K., & Raissy, H. (2018). Asthma guidelines from the National Asthma Education and Prevention Program: Where are we now? Pediatric Allergy, Immunology, And Pulmonology, 31(1), 37-39. doi: 10.1089/ped.2018.0878
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Klok, T., Kaptein, A., & Brand, P. (2015). Non-adherence in children with asthma reviewed: The need for improvement of asthma care and medical education. Pediatric Allergy and Immunology, 26(3), 197-205. doi: 10.1111/pai.12362
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Milligan, K., Matsui, E., & Sharma, H. (2016). Asthma in urban children: Epidemiology, environmental risk factors, and the public health domain. Current Allergy and Asthma Reports, 16(4). doi: 10.1007/s11882-016-0609-6
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Mims, J. (2015). Asthma: Definitions and pathophysiology. International Forum of Allergy & Rhinology, 5(S1), S2-S6. doi: 10.1002/alr.21609
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Wang, G., Zhang, X., Zhang, H., Wang, L., Kang, D., Barnes, P., & Wang, G. (2017). Corticosteroid plus ²2-agonist in a single inhaler as reliever therapy in intermittent and mild asthma: A proof-of-concept systematic review and meta-analysis. Respiratory Research, 18(1). doi: 10.1186/s12931-017-0687-6
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